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Review article
Indoor PM2.5, tobacco smoking and chronic lung diseases: A narrative review Yingmeng Nia,b,1, Guochao Shia,b,1, Jieming Qua,b,∗ a b
Department of Pulmonary and Critical Care Medicine, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China Institute of Respiratory Diseases, Shanghai Jiao Tong University School of Medicine, Shanghai, China
A R T I C LE I N FO
A B S T R A C T
Keywords: Environment tobacco smoke Indoor PM2.5 Lung cancer COPD Asthma Chronic lung diseases
The lung is one of the most important organs exposed to environmental agents. People spend approximately 90% of their time indoors, and risks to health may thus be greater from exposure to poor air quality indoors than outdoors. Multiple indoor pollutants have been linked to chronic respiratory diseases. Environmental tobacco smoke (ETS) is known as an important source of multiple pollutants, especially in indoor environments. Indoor PM2.5 (particulate matter with aerodynamic diameter < 2.5 μm) was reported to be the most reliable marker of the presence of tobacco smoke. Recent studies have demonstrated that PM2.5 is closely correlated with chronic lung diseases. In this paper, we reviewed the relationship of tobacco smoking and indoor PM2.5 and the mechanism that underpin the link of tobacco smoke, indoor PM2.5 and chronic lung diseases.
1. Introduction The adult human lung has an approximate gas exchange surface area of 100 m2, and inhales and exhales over 10,000 L of air per day when resting (Thatcher et al., 2019). As such, the lung is one of the most important organs exposed to environmental agents. Meanwhile, the lung receives the whole blood, thus, environmental agents may injure various hemocytes and lead to systemic inflammation (Xu et al., 2016). People in many countries spend more than 90% of their time indoors, and risks to health may thus be greater from exposure to poor air quality indoors than outdoors (Abramson et al., 2015). Multiple indoor pollutants have been linked to chronic respiratory diseases. Environmental tobacco smoke (ETS) is known as an important source of multiple pollutants, especially in indoor environments (Kauneliene et al., 2018; Muller et al., 2011). Tobacco smoke is similar to other combustion-sourced pollutants, including carbon particulates, partially combusted hydrocarbons, LPS and other biological products, and gasses such as ammonia (Roemer et al., 2004). Indoor PM2.5 (particulate matter with aerodynamic diameter < 2.5 μm) was reported to be the most reliable marker of the presence of tobacco smoke (7). Recent studies have demonstrated that PM2.5 is closely correlated with chronic lung diseases (Guan et al., 2016; Schraufnagel et al., 2019; Wei and Tang, 2018). In this paper, we reviewed the relationship of tobacco smoking and
indoor PM2.5 and the mechanism that underpin the link of tobacco smoke, PM2.5 and chronic lung diseases. Considering incidence and disease burden, lung cancer, asthma, chronic obstructive pulmonary disease, interstitial lung diseases and tuberculosis were discussed in this review Tables 1 and 2. 2. Indoor PM2.5 and ETS PM refers to the dispersed solid, liquid or solid-liquid suspensions in the air (Wilson JCC et al., 2002). The diameter, composition, and origin of PM determine the toxicity and biological pathogenicity (Valavanidis et al., 2008). Since the small diameter of PM2.5, it can go deep to the distal airways and deposits in alveolar regions and do ineligible harm to human respiratory system (Brunekreef and Holgate, 2002). The sources of indoor PM2.5 differ from outdoor PM2.5. Habre et al. compared the components of indoor PM2.5 and outdoor PM2.5. The elemental carbon (EC) components of indoor PM2.5 originate from smoldering combustion (Habre et al., 2014a), as found during tobacco smoking and using fireplaces. On the other hand, the EC components of PM2.5 from outdoor sources originate mainly from internal-combustion engine exhaust soot. In high-income countries, ETS is considered as the main source of toxic chemical species, both gaseous and particulate phase, in indoor environments. Drago et al. (2018) studied 73 houses in Italy and found
∗
Corresponding author. No. 197, Ruijin Er Road, Shanghai, 200025, China. E-mail address:
[email protected] (J. Qu). 1 These authors contributed equally. https://doi.org/10.1016/j.envres.2019.108910 Received 3 September 2019; Received in revised form 5 November 2019; Accepted 7 November 2019 0013-9351/ © 2019 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/BY-NC-ND/4.0/).
Please cite this article as: Yingmeng Ni, Guochao Shi and Jieming Qu, Environmental Research, https://doi.org/10.1016/j.envres.2019.108910
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Abbreviation: ETS PM2.5 EC PM10 RR NSCLC IL MMP-1 COPD AECOPD PEF OR OS NF-kB
TNF GM-CSF BMI FEV1 FVC FEF25-75 TSLP ILD DIP PLCH IPF TGF-β ACPAs TB
environmental tobacco smoke particulate matter with aerodynamic diameter <2.5 μm elemental carbon particulate matter with aerodynamic diameter <10 μm relative risk non-small cell lung cancer interleukin matrix metalloproteinase-1 chronic obstructive pulmonary disease acute exacerbation of COPD peak expiratory flow odd ratio oxidative stress nuclear factor kappa-light-chain-enhancer of activated B
cells tumor necrosis factor granulocyte-macrophage colony-stimulating factor body mass index forced expiratory flow at 1 s forced vital capacity forced expiratory flow at 25–75% of forced vital capacity thymic stromal lymphopoietin interstitial lung diseases desquamative interstitial pneumonia pulmonary Langerhans cell histiocytosis idiopathic pulmonary fibrosis transforming growth factor beta anti-citrullinated protein antibodies tuberculosis
over 24 h and 1 year (Brunekreef and Holgate, 2002), it should be note that there is no safe level of exposure to ETS or PM2.5.
that concentrations of PM2.5, Cadmium, Cerium, Lanthanum, and Thallium were significantly higher in smoker dwelling than non-smoker dwelling. This study also showed that indoor PM2.5 was the most reliable marker of the presence of tobacco smoke. The smoking household's PM2.5 levels showed dynamic response to the smoking events. It can have a peak up to 400–1000 μg m−3 some minutes after smoking events (Russo et al., 2015). Another study focused on the effect of smoking on indoor air quality during sleeping (Canha et al., 2019). PM2.5 and PM10 were monitored in 10 different bedrooms. Concentration of PM2.5 and PM10 of smokers' bedrooms was 61.2 ± 24.4 μg m−3 and 67.5 ± 22.8 μg m−3 respectively, while for non-smokers the value was around 6 times lower for both PM2.5 and PM10 (8.9 ± 7.0 μg m−3 and 11.0 ± 6.9 μg m−3, respectively). PM2.5 can absorb organic molecules, transition metals, reactive gases, microbial components, and indoor allergens, serving as a carrier for these potentially harmful molecules (Chien and Huang, 2010; Pennanen et al., 2007). It is suggested that > 90% of the total harm caused by the ETS pollutants was due to PM2.5 (Sleiman et al., 2014). However, it should be note that, in low-income countries, other sources of pollution are more important, such as biomass burning (Yin et al., 2019). Recently, another exposure route emerged to add the cumulative burden of tobacco exposure, particularly in indoors environments: third-hand tobacco smoke (THS). Tobacco smoke residues can linger in the indoor environment and become a source of long-term exposure to harmful pollutants. PM2.5 can remain airborne or be absorbed to indoor surfaces and dust particles and stay for many hours after smoking has ended. In one model, the disability-adjusted life years (DALYs) lost annually by 100,000 nonsmokers exposed to ETS, including THS, was estimated to be about 1520 years when smoker was away from home most of the day and non-smoker was at home (Sleiman et al., 2014). As the use of electronic cigarettes device, including IQOS and ecigarettes, continue to grow in popularity among adolescents and adults, increasing researches explore the relationship between PM2.5 and electronic cigarettes aerosol. Research reveals that the aerosol produced from e-cigarette use contains toxicants including nicotine, glycols, aldehydes, metals, volatile organic compounds, and polycyclic aromatic hydrocarbons. Studies showed that during the vaping of ecigarettes, indoor PM2.5 could elevated to 197–818 μg/m3 (Soule et al., 2017). This level of PM2.5 is comparable or even higher than the level that conventional cigarettes can induce. Smoking of an IQOS has little effect on the concentration of fine particles (> 300 nm) or on the PM2.5 concentration in the indoor environments. However, the concentration of ultrafine particles (25–300 nm) can be markedly increased (Schobera et al., 2019). The importance of this finding for the health of passive smokers is currently unclear. Although WHO and US Environmental Protection Agency give a suggestion of allowed maximum concentration of PM2.5 when averaged
3. ETS, PM2.5 and lung cancer 3.1. Epidemiology The British Doctors' Study (Doll, 1954) is the most long-standing prospective cohort study on tobacco and health hazards, including lung cancer. The researchers published a 20-year follow-up study in 1976, a 40-year follow-up in 1994, and a 50-year follow-up in 2004 (Doll, 1954, 1976; Doll et al., 1994). The relative risk (RR) of smoking for lung cancer mortality was increased over the duration of follow-up. The RR was approximately 8 at the time of the 20-year follow-up study and increased to over 14 after 40-year follow-up. In 1950's, the US veteran cohort study (Doll et al., 2004) was started and showed that the RR of smoking for lung cancer mortality was 11.7 (95% CI 10.1–13.7). Although RRs were relative lower, studies in Asian region also showed increased risk of lung cancer in smokers. One Chinese study (McLaughlin et al., 1995) interviewed the surviving family members of one million people who died from 1986 to 1998 in 98 areas of China, and found that the lung cancer mortality was about 2.57 (SE = 0.07) times higher in smokers than in nonsmokers among men and 1.98 (SE = 0.13) times greater in smokers than in non-smokers in women. The Japan Collaborative Cohort (JACC) study (Liu et al., 1998) showed that the RRs of smoking for lung cancer mortality were 4.46 (95% CI 3.10–6.41) in men and 3.58 (95% CI 2.24–5.73) in women. In Korean Cancer Prevention Study (KCPS) (Ando et al., 2003), the RRs of smoking for lung cancer were 4.6 in men and 2.5 in women. The relative lower RR in Asian studies may be due to epidemiologic differences between Western and Asian populations, such as smaller smoking amount and late age of smoking initiation in Asian countries. Lung cancer in never-smokers is the seventh most common cause of cancer-mortality. Lung cancer in never-smokers shows a different age of diagnosis, stage at presentation, histological composition, and survival outcome, thus it is regarded as a distinct disease differ from smoking related lung cancer (Jee et al., 2004; Rudin et al., 2009; Sun and Gazdar, 2007). About 25% of lung cancer globally occurs in neversmokers (Toh et al., 2006), of which 4.2 and 6.7% in males and females were attributable to passive ETS resulting from their partner's active smoking (Ferlay et al., 2008). Kim AS et al. (Kim et al., 2018) carried out a meta-analysis recruiting 40 studies about passive ETS exposure and the prevalence of cancer. In this meta-analysis, 12 studies were about lung cancer. Results showed that RR of passive ETS exposure for lung cancer prevalence was 1.25 (95% CI 1.10–1.39, p < 0.001).
2
3
Cohort
2007 2015
2017 2013
2015
2004
Yin P, (Yin et al., 2007) Cortez-Lugo M, (Cortez-Lugo, 2015)
Sun X, (Sun et al., 2018) Hansel N, (Hansel et al., 2013)
Asthma Coogan P, (Coogan et al., 2015)
Jaakkola JJ, (Jaakkola, 2004)
Cohort
Cohort
Cohort Cohort
Cross-sectional Cohort
Cross-sectional
2003
Ando M, (Liu et al., 1998)
Retrospective proportional Cohort
2019
1998
Liu B, (McLaughlin et al., 1995)
Cohort
Meta-analysis
1995
McLaughlin JK, (Doll et al., 2004)
Cohort
2018
2004
Doll R, (Doll et al., 1994)
Cohort
Kim AS, (Kim et al., 2018) COPD Zha Z, (Zha et al., 2019)
1994
Doll R, (Doll, 1976)
Cohort
2004
1976
Lung Cancer Doll R, (Doll, 1954)
Design
Jee SH, (Ando et al., 2003)
Year
First author, reference
Table 1 Epidemiology studies included in the review.
7 years
14.7 years
10 months 6 months
/ 10 months
/
/
24 years
7 years
/
26 years
50 years
40 years
20 years
Follow-up period
Maternal smoking
ETS
Outdoor PM2.5 Indoor PM2.5
Active smoking, indoor exposure to coal ETS Outdoor PM2.5
Passive ETS
Active smoking
Active smoking
Active smoking
Active smoking
Active smoking
Active smoking
Active smoking
Exposure/intervention
Asthma prevalence
Adult-onset asthma incidence
Monthly episodes of AECOPD COPD symptoms, AECOPD, severe AECOPD
COPD prevalence, lung function Peak expiratory flow
Lung function, COPD prevalence
Cancer prevalence
Lung cancer mortality
Mortality from neoplastic, respiratory or vascular disease Lung cancer mortality
Total and site-specific cancer mortality
All cause mortality, disease specific mortality
All cause mortality, disease specific mortality
All cause mortality, disease specific mortality
Health outcomes
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The multivariable HRs for former active smoking, current active smoking, and passive smoking only were, respectively, 1.36, 1.43, and 1.21, compared with never active/passive smoking. OR of maternal smoking for asthma prevalence was 1.35.
OR of current smoking for COPD prevalence was 2.63, OR of indoor exposure to coal for COPD prevalence was 1.55. OR of ETS for COPD prevalence was 1.48. For a 10-μg/m3 increase in PM2.5, there was a significant 33% increase in cough (95% CI, range, 5–69%), and 23% in phlegm (95% CI, range, 2–54%), a reduction of the PEF average in the morning of −1.4 L/min (95% CI, range, −2.8 to −0.04), and at night of −3.0 L/min (95% CI, range, −5.7 to −0.3), respectively. OR of per 10μg/m3 increment in PM2.5 for AECOPD was 1.09. OR of per 10 mg/m3 increase in indoor PM2.5 for nocturnal respiratory symptoms was 1.44, and for risk of severe COPD exacerbations was 1.50. Increase in indoor PM2.5 was correlated with increased rescue medication use (β = 0.11,95% CI = 0.02–0.20, p = 0.01)
Age standardized annual lung cancer mortality per 100,000 men of lung cancer was 10 in non-smokers, 83 in current or former smokers. Age standardized annual lung cancer mortality per 100,000 men of lung cancer was 14 in non-smokers, 58 in former smokers and 209 in current smokers. Age standardized annual lung cancer specific mortality per 1000 men was 0.17 in non-smokers, 0.68 in former smokers and 2.49 in current smokers. RR for all cause mortality was 1.7. RRs for lung cancer mortality were 11.7. RRs for lung cancer mortality were 3.7 in current smokers with 1–9 cigarettes per day, 9.9 in current smokers with 10–20 cigarettes per day, 16.9 in current smokers with 21–39 cigarettes per day, and 22.9 in current smokers with 40 + cigarettes per day. RRs for lung cancer mortality were 2.57 in man and 1.98 in women. RRs for lung cancer mortality were 2.38 in male ex-smokers, 4.46 in male current smokers, 2.56 in female ex-smokers, and 3.58 in female current smokers. RRs for lung cancer mortality were 2.3 in smokers with < 10 cigarettes per day, 3.2 in smokers with 10–19 cigarettes per day, 5.2 in smokers with 20–29 cigarettes per day, and 7.9 in smokers with ≥ 30 cigarettes per day. RRs for lung cancer mortality were 4.6 in men and 2.5 in women. RR of passive ETS for lung cancer prevalence was 1.25.
Main findings
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2018
2019
Accordini S, (Accordini et al., 2018)
Isiugo K, (Isiugo et al., 2019)
1997
2017
2017
2009
2007
Interstitial lung diseases Baumgartner KB, (Baumgartner et al., 1997)
Sack C, (Sack et al., 2017)
Sese L, (Sack et al., 2017)
Tuberculosis Kolappan C, (Kolappan, 2009)
Slama K, (Slama et al., 2007)
2011
2014
Fuentes-Leonarte V, (FuentesLeonarte et al., 2015)
McCormack M, (McCormack et al., 2011)
2005
Skorge TD, (Skorge et al., 2005)
2014
2005
Li YF, (Li et al., 2005)
Habre R, (Habre et al., 2014b)
Year
First author, reference
Table 1 (continued)
Meta-analysis
Case-control
Cohort
Cohort
Case-control
Cohort
Cohort
Cohort
Cross-sectional
Cohort
Cohort
Case-control
Design
/
/
5 years
10 years
/
6 months
2 years
2 years
/
1 year
11 years
/
Follow-up period
ETS, biomass fuel usage, alcohol consumption ETS
Air pollution (PM2.5, PM10, O3, NO2)
Ambient pollution (PM2.5, NOx, NO2 and O3)
Active smoking
Indoor PM2.5
Indoor and outdoor PM2.5
Exposure to black carbon, ultraviolet absorbing particulate matter (UVPM), PM2.5 or fungi
Paternal smoking
Prenatal and postnatal ETS
Maternal smoking in utero and ETS in childhood
Maternal smoking, postnatal ETS, grandmaternal smoking
Exposure/intervention
TB infection, developing TB disease, mortality from TB
Tuberculosis prevalence
IPF mortality
Interstitial lung abnormalities and high attenuation area of computed tomography
IPF incidence
Asthma symptoms, rescue medication use
Lung function
Offspring's asthma prevalence
Occurrence of otitis, cough persisting for more than 3 weeks, lower respiratory tract symptoms, and lower respiratory tract infections.
(continued on next page)
OR of smoking for being infected with TB was 1.76. OR of smoking for developing TB disease was 3.35. OR of passive ETS for developing TB disease was 2.28. OR of smoking for TB mortality was 2.24.
OR of biomass fuel usage for tuberculosis was 1.7.
The odds ratio (OR) for ever smoking was 1.6. Risk was significantly elevated for former smokers (OR = 1.9) and for smokers with 21–40 pack-yr (OR = 2.3). The OR of per 40 ppb increment in NOx for ILA was 1.62 in total cohort and was 2.60 in non-smokers. HAA increased by 0.54% per year per 5μg/m3 increment in PM2.5 and by 0.55% per year per 40 ppb increment in NOx. IPF mortality was significantly associated with increased cumulative exposure to PM10 with an HR of 2.01 per 10 μg/m3 and to PM2.5 with a HR of 7.93 per 10 μg/m3
OR of maternal smoking for asthma prevalence in the first 5 years of life was 1.5. OR of grandmaternal smoking for grandchildren asthma prevalence in the first 5 years of life was 2.1. Maternal smoking was associated with asthma, phlegm cough, chronic cough, dyspnea grade 2, attacks of dyspnea, and wheezing, with odds ratios of 3.0, 1.7, 1.9, 1.9, 2.0, and 1.4, respectively. The adjusted attributable fractions of the adult incidence of asthma were 17.3% caused by maternal smoking and 9.3% caused by smoking by other household members. Maternal smoking during pregnancy increased the odds for wheezing (OR: 1.41) and chETSiness (OR: 1.46). Postnatal exposure from fathers was associated with otitis (OR: 1.25). Passive exposure at work of non-smoking mothers during pregnancy was related to cough (OR: 1.62). Fathers' smoking before they were 15 (RR = 1.43) and mothers' smoking during pregnancy (RR = 1.27) were associated with asthma without nasal allergies in their offspring. Grandmothers' smoking during pregnancy was associated with asthma in their daughters (OR = 1.55) and with asthma with nasal allergies in their grandchildren within the maternal line (RR = 1.25). 11.3 μg/m3 increase in indoor UVPM was associated with 6.4% and 14.7% decrease in percent predicted FEV1/FVC ratio and FEF25–75 respectively. 17.7 μg/m3 increase in indoor PM2.5 was associated with 6.1% and 12.9% decrease in percent predicted FEV1/FVC ratio and FEF25–75, respectively. ORs of PM2.5 from indoor sources were 1.24 for cough and 1.63 for wheeze in asthma patients. RRs of indoor PM 2.5 were 1.12 for limited speech and 1.09 for rescue medication use in non-atopic asthma children. RRs of indoor PM 2.5 were 1.07 for slow down, 1.07 for symptoms with running, and 1.09 for nocturnal symptoms in atopic asthma children.
Asthma prevalence in the first 5 years of life
Asthma symptoms and prevalence
Main findings
Health outcomes
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3.2. Mechanism
Active TB, latent TB infection, TB mortality
TB infection, TB disease
ETS, indoor air pollution
Passive ETS
OR of smoking for latent TB was 2.08, OR of passive ETS for latent TB was 2.68. OR of current smoking for pulmonary TB was 2.01. OR of former smoking for pulmonary TB was 1.68. OR of ever smoking for Pulmonary TB was 3.28. OR of ETS for TB mortality was 2.32. OR of passive ETS for TB disease was 1.59.
Health outcomes
A large amount of DNA adducts formation is an early molecular sign of exposure to ETS. Electrophilic compounds bind to the nucleophilic sites of DNA nucleotides and lead to the DNA adducts formation (Jung et al., 2016). DNA adducts cause point mutations, especially in proliferating cells. The next early molecular event of ETS exposure is the gene mutations, targeting key oncogenes for carcinogenesis (Izzotti and Pulliero, 2015). Mitochondrial DNA is also a target of tobacco smoke genotoxicity. Since the mitochondria has lower power of DNA repair and does not have a histone packaging, mitochondrial DNA becomes more sensitive than nuclear DNA to genotoxicity (Yao et al., 2005). In addition to DNA, tobacco smoke has a profound effect on microRNA expression. Izzotti et al. investigated 484 microRNAs expression level in the lung of rats, showing that 126 microRNAs were down regulated more than 2-fold and 24 microRNAs more than 3-fold after exposure to tobacco smoke of 4 weeks (Izzotti, 2009). PM2.5 exposure leads to DNA alteration by modifying methylation level of genes. The classic oncogene, p53, plays an important role in cell proliferation, apoptosis and damage repair (Izzotti et al., 2009). Mutation of p53 contributes to the pathogenesis of lung cancer (Cai et al., 2013; Ellis et al., 1997). PM2.5 is able to trigger p53 promoter methylation by increasing DNA (cytosine-5-)-methyltransferase 3β (DNMT3B) methylation levels, resulting in p53 inactivation (Zhou et al., 2016). Notably, these cells were exposed to a ‘safe’ concentration of PM2.5 (120 μg/m3) that was comparable to a daily exposure in the north area of China in 2011. Another study about the methylome and transcriptome of PM2.5-treated (100 μg/ml) BEAS-2B cells identified 66 differentially expressed genes, of which the methylation levels were either increased or decreased (Heßelbach et al., 2017). The tumor microenvironment is of importance to lung cancer development (Graves, 2010). Varied inflammatory cytokines and transcription factors orchestrate in the lung cancer microenvironment (Cho et al., 2011). ETS is reported to be able to over activate immune cells, including macrophages, dendritic cells, lymphocytes, and granulocytes (O'Callaghan et al., 2010). Exposure to PM2.5 induces epithelial cells and macrophages activation, releasing various pro-inflammatory cytokines, including IL-6, TNF-α and granulocyte-macrophage colony stimulating factor (GM-CSF) (Baulig et al., 2007; Gualtieri et al., 2008). It is also reported that PM2.5 exposure increased the mobility and proliferation of A549 and H1299 cells, and IL-1β and MMP-1 may be involved (Yang et al., 2016). These studies indicate that tobacco smoke, as well as PM2.5 exposure, lead to an inflammatory microenvironment that is facilitate the proliferation of malignantly transformed cells.
/
4. ETS, PM2.5 and chronic obstructive pulmonary disease (COPD) /
Follow-up period
Exposure/intervention
Main findings
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COPD results from a complex interaction between genes and the environment (Global Initiative for Chr, 2019). Tobacco smoking is the most commonly risk factor for COPD. Smokers have a higher prevalence of respiratory symptoms and lung function abnormalities (Kohansal et al., 2009). In a recent Chinese study (Zha et al., 2019), a survey was conducted in a population aged 40 years or older. Results from 2770 participants showed that current smoking had an odds ratio (OR) of 2.63 (95% CI 1.86–3.73) for COPD. Passive exposure to ETS may also contribute to COPD by elevating total burden of inhaled particles and gases of lungs (Yin et al., 2007). In a lung function trajectories study, Bui et al. modeled lung function trajectories based on the cohort from the Tasmanian Longitudinal Health Study (TAHS) (Dinh S Bui Burgesset al., 2018). Results showed that maternal smoking was a risk factor of adult COPD and personal smoking increased the impact of maternal smoking. Numerous studies have demonstrated that COPD and acute exacerbation of COPD (AECOPD) are associated with air pollution,
2015 Dogar OF, (Dogar OF et al., 2015)
Meta-analysis
2007 Lin HH, (Lin and Murray, 2007)
Meta-analysis
Year First author, reference
Table 1 (continued)
Design
4.1. Epidemiology
5
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Table 2 Mechanisms that underpin the link of ETS, indoor PM2.5 and chronic lung diseases. Disease
ETS
PM2.5
Lung cancer
DNA adducts formation Point mutations Mitochondrial DNA damage Impaired microRNA expression Increased oxidative stress Increase of pro-inflammatory cytokines and chemokines Bacterial colonization
Hypermethylation of oncogene Tumor microenvironment
COPD
Asthma
Interstitial lung diseases
Tuberculosis
Th1 to Th2 shift Impaired lung deposition and function of antigen presenting cells Impaired B cell function Epithelial cell-derived cytokines and chemokines Inhibition of autophagy Mitochondria damage Impaired histone acetylation and methylation Anti-citrullinated protein antibodies Impaired function of alveolar macrophage Impaired neutrophil influx and activation Decreased Th1 numbers and IFN-r production Enhanced Treg function
Increase of pro-inflammatory cytokines and chemokines Systemic inflammation Impaired microbiome Reduce of bacterial elimination Increase of pro-inflammatory cytokines and chemokines Adjuvant Allergen carrier Systemic inflammatory response
Reduce cytokines production (IL-1β, TNF-α)
13 (Hong et al., 2016). PM2.5 may also stimulate alveolar macrophages (AM) to secrete inflammatory mediators such as arachidonic acid, TNFα, and IL-6 (Pozzi et al., 2003), and impair the phagocyte of AM (Li et al., 2018). Systemic inflammation is highly associated with the incidence and progression of COPD (Groenewegen et al., 2008). PM2.5 contributes to the systemic inflammatory response and the functional alteration of multiple organs (van Eeden et al., 2005). Indoor PM2.5 exposure leads to urinary metabolite alterations, which are shown to be closely related to COPD by metabolic pathway analysis (Huang et al., 2018). Golpe et al. (2017) compared the systemic inflammation level between tobacco-induced COPD (T-COPD) and biomass smoke-induced COPD (BCOPD). The results showed that T-COPD patients had higher serum IL-6 and IL-8 levels than patients with B-COPD, indicating a higher level of systematic inflammation. Bacterial colonization is commonly observed in the lower airway of COPD patients. Tobacco smoking is reported to increase the translocation of S. pneumoniae into the lung (Voss et al., 2015). This translocation is associated with increased concentrations of inflammatory mediators and overactivation of immune cells in lavage fluids of the upper respiratory tract and the lung (Voss et al., 2015). PM2.5 increases the risk of bacterial infections in COPD patients via different mechanisms. Researchers found that PM2.5 particles carry bacteria or bacteriaderived components (Menetrez et al., 2001; Alghamdi et al., 2014). Therefore, they may break the balance of the microbiome in the distal airway of COPD patients and subsequently lead to AECOPD. PM2.5 exposure was also found to promote pneumococcal adhesion to human epithelial cells, thereby increasing pneumococcal pneumonia susceptibility (Mushtaq et al., 2011). In addition, PM2.5 in diesel exhaust reduces bacterial elimination from the lungs by suppressing the production of LPS-stimulated proinflammatory cytokines and weakening phagocytosis (Castranova et al., 2001).
particularly PM2.5. Long-term exposure to traffic emissions and outdoor PM2.5 has been demonstrated to decrease FEV1 and FVC, and accelerate the decline in lung function in healthy adults in a population-based cohort (Rice et al., 2015). Each additional 10 μg/m3 PM2.5 exposure has been reported to increase the rate of cough by 33% (95% CI 5–69%) and sputum by 23% (95% CI 2–54%) in COPD patients, and to decrease the average PEF by 1.4 L/min (95% CI 0.04–2.8) in the morning and by 3.0 L/min (95% CI 0.3–5.7) at night (Cortez-Lugo, 2015). Sun et al. (2018) showed a positive correlation between the monthly episodes of AECOPD and the concentrations of outdoor PM2.5 (r = 0.884, p < 0.05). The OR of per 10 μg/m3 increase in PM2.5 was 1.09 (95% CI 1.07–1.11, p < 0.001) for AECOPD. Individuals with COPD spend more time at home than their age-matched counterparts(59). Indoor air quality is especially important for COPD patients. One study showed that per 10 mg/m3 increase in indoor PM2.5 concentration in the main living area was associated with increase in nocturnal respiratory symptoms (OR = 1.44, 95% CI 0.006–0.24, p = 0.01), rescue medication use (β = 0.11, p = 0.01), and risk of severe COPD exacerbations (OR = 1.50, 95% CI 1.04–2.18, p = 0.03) (Hansel et al., 2013), which is more closely related than outdoor PM2.5.
4.2. Mechanism Previous research has shown increased oxidative stress (OS) and enhanced catalase activity in COPD subjects (Wijnhoven et al., 2006; Zuo et al., 2012). OS plays an important role in the airway inflammation that is a key feature in COPD. Tobacco smokers have been found to have a greater level of oxidative stress (MacNee, 2005a, 2005b), which is most likely attributed to the high concentration of oxidants in tobacco smoke (Zuo et al., 2014). PM2.5 has also been reported to be able to induce lung oxidative stress and inflammation in healthy mice, even at a low dose (Malm et al., 2011). The oxidative stress facilitates the binding of NF-kB to DNA, resulting in increased mRNA expression of NF-kB-related downstream inflammatory cytokines such as TNF-α, TNF-β, and IL-6 in murine alveolar type II epithelial cells (Shukla et al., 2000) and IL-8 in human airway cells (Yan et al., 2016). Increased expressions of pro-inflammatory cytokines and chemokines accelerate the inflammatory reaction. Exposure to tobacco smoke in vitro induces the release of IL-1β from human airway epithelial cells (Mortaz et al., 2011). In parallel, the level of IL-1β is elevated in the serum of smokers and is considered to be important in the development of chronic airway inflammation (). PM2.5 exposure can activate human nasal epithelial cells and lead to the release of GM-CSF, TNF-α, and IL-
5. ETS, PM2.5 and asthma 5.1. Epidemiology Both active smoking and passive exposure to ETS were associated with an increased incidence of adult-onset asthma. Coogan et al. (2015) followed 46,182 participants from 1995 to 2011 and showed that the multivariable HRs of former active smoking, current active smoking, and passive exposure to ETS only for asthma were, respectively, 1.36 (95% CI 1.11–1.67), 1.43 (95% CI 1.15–1.77), and 1.21 (95% CI 6
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airway, and lead to further airway allergic inflammation (Pace EF et al., 2014; Montano-Velazquez BBF-R et al., 2017; Mulligan JKOC et al., 2017). PM2.5 induced airway inflammation and immune system impairment in asthma are similar as in COPD. However, the role of PM2.5 as a carrier is particularly important in asthma. Metals, such as Fe, Pb, Cu, As, Mo and Cd, carried by PM2.5 are reported to be involved in murine lung eosinophilic inflammation (He et al., 2019). One study on a guinea pig model of allergic asthma also showed that acute inhalation of concentrated PM2.5 from Mexico City could act as an adjuvant to trigger the allergic lung inflammation (Falcon-Rodriguez et al., 2017). Furthermore, pollen grains or plant-derived paucimicronic components may interact with PM in producing allergic symptoms. In a European study, allergens from pollens, latex and β-glucans were reported to bind to ambient air particles (D'Amato and Cecchi, 2008). In a Japanese study, PM2.5 was found to be able to significantly enhance the association between airborne pollen and daily clinic visits for pollinosis in Fukuoka (Phosri et al., 2017).
1.00–1.45), compared with never exposure to ETS. A dose-response relationship between asthma and smoking was found among both former and active smokers. (Coogan et al., 2015; Moazed, 2015). It is widely accepted that mothers' smoking during pregnancy increases the risk of asthma and asthma-like symptoms in their offspring (Jaakkola, 2004; Li et al., 2005; Skorge et al., 2005; Fuentes-Leonarte et al., 2015). A three-generation study (Accordini et al., 2018) conducted in Europe revealed that fathers' smoking before the age of 15 was also associated with an increased risk of asthma (RR = 1.43, 95% CI 1.01–2.01), suggesting an effect of paternal pre-adolescent smoking on the next generation. Moreover, grandmothers’ smoking during pregnancy was associated with an increased risk of asthma in their grandchildren within the maternal line (RR = 1.25, 95% CI 1.02–1.55), suggesting a multi-generation effect of tobacco smoking. An epidemiologic study of inner-city children with asthma showed that the major indoor source for PM2.5 from these children's homes was smoking, which elevated indoor concentrations by 37 μg/m3 in the 101 homes with smokers (Wallace et al., 2003). Meanwhile, the same study found that outdoor PM2.5 was responsible for only 25% of the mean indoor PM2.5 concentration. Indoor PM2.5 exposure is found to be responsible for lung function impairment in asthmatic children (Isiugo et al., 2019; Habre et al., 2014b). An increase of 17.7 μg/m3 in indoor PM2.5 was associated with 6.1% (99% CI 2.4–10.4) and 12.9% (99% CI 1.0–24.9) decrease in predicted FEV1/FVC ratio and FEF25–75, respectively (Isiugo et al., 2019). Interestingly, it is shown in the same study that outdoor PM, indoor black carbon, and indoor fungal spores were not significantly associated with lung function (Isiugo et al., 2019). In-home particle concentration has also been shown to be associated with asthma morbidity, including symptoms and rescue medication use, among not only atopic but also non-atopic children (McCormack et al., 2011).
6. ETS, PM2.5 and other chronic lung diseases 6.1. Interstitial lung diseases In recent years, attention has also focused on the role of smoking in the development of interstitial lung diseases (ILDs). Given the different associations with tobacco smoking, Vassallo et al. (Vassallo, 2012) proposed an ILD classification. Respiratory bronchiolitis-associated ILD (RB-ILD), desquamative interstitial pneumonia (DIP) and pulmonary Langerhans cell histiocytosis (PLCH) are strongly etiologically linked to smoking. Idiopathic pulmonary fibrosis (IPF) and rheumatoid arthritisrelated ILD (RA-ILD) have a higher prevalence in smokers. In IPF, smoking is now considered a risk factor (Margaritopoulos et al., 2013). Current or former smokers have about 60% higher risk of developing IPF than non-smokers (OR 1.6, 95% CI 1.1–2.4) (Baumgartner et al., 1997). Low levels of autophagy may be an important factor (Patel et al., 2012). The inhibition of autophagy is suggested to be induced by the activation of phosphatidylinositol-3 kinase and the mammalian target of rapamycin. Another study by the same authors (Patel et al., 2015) demonstrated that mitochondria were damaged in IPF lungs, and mitochondrial depolarization was induced by TGF-β treated lung epithelial cells. Smoking induces TGF-β production, thus, may suppress autophagy and mitophagy. Other studies suggested that tobacco smoke induced impaired histone acetylation and histone hypermethylation might also have a role in the fibrogenic process in IPF (Coward et al., 2009, 2010). In rheumatoid arthritis, it is found that patients with anti-citrullinated protein antibodies (ACPAs) are more likely to have lung abnormalities (Lake, 2014). The citrullination is a smoking triggered post-translational modification of proteins and can lead to protein structure alteration and functional consequences. PM2.5 also showed influences on the natural history of ILD. Sack et al. (Li et al., 2019) analyzed the cardiac CT scans results from MultiEthnic Atherosclerosis Study (MESA) cohort, and found that per 5 μg/ m3 increment in outdoor PM2.5 increased the prevalence of high attenuation areas on CT scans by 0.54% (95% CI 0.02–1.10, p = 0.04), indicating a relationship between PM2.5 and subclinical ILD. Another study showed that the mortality of IPF was significantly associated with increased levels of exposure to outdoor PM2.5 per 10 μg/m3 (HR = 7.93, 95% CI 2.93–21.33, p < 0.001) (Sack et al., 2017). The PM2.5-induced systemic inflammatory response could be the most relevant mechanism (Sese et al., 2018).
5.2. Mechanism Exposure to tobacco smoke was highly related to sensitization to cockroaches, grass pollen, and certain food allergens in children (Yao TCC et al., 2016). Exposure to ETS can alter the immune functions of various immune cells and aggravate allergic inflammation and sensitization (Cheraghi MS, 2009; Botelho et al., 2010; Smith LAP et al., 2010; Robays LJM et al., 2009; Zavitz et al., 2008; Van Hove CLM et al., 2008). Exposure to ETS impaired lung deposition of antigen-presenting cells and their production of IFN-γ, TNF-α, IL-12, and RANTES, thus inhibiting the recruitment of Th1 polarized cells to the lung. Meanwhile, exposure to ETS enhanced Th2 responses in the lung, initiating the shift in T-cell polarization upon entering the lung. Th1 to Th2 shift may favor the development of allergic diseases such as asthma (Shaler CRH et al., 2013; Strzelak et al., 2018). The classic atopic asthma is an IgE mediated disease. Growing evidence supports the linkage between parental smoking and atopy in children, including increased serum IgE level, eosinophilia, and positive skin-prick tests (Kulig ML et al., 1999). Adult active smokers were also found to have an elevated serum IgE level (Oryszczyn et al., 2000). However, studies suggest that B-cell development, function, and immunoglobulin production are suppressed in smokers (Brandsma CAH et al., 2009). Although the memory B-cell percentages in peripheral blood were decreased, current smokers showed higher percentages of class-switched memory B cells than non-smokers. This may explain the elevated serum IgE level in active smokers (Strzelak et al., 2018). Exposure to ETS also leads to increased permeability of the respiratory epithelium, impaired mucociliary clearance, and release of epithelial cytokines and chemokines (Cohen NAZ et al., 2009; Olivera DK et al., 2010; Kanai KK et al., 2015; Pace EF et al., 2008; Damia ADG et al., 2011). The increased permeability facilitates the infiltration of allergens (Gangl KR et al., 2009). Cytokines and chemokines released by epithelial cells, including IL-33, TSLP, GM-CSF, can recruit neutrophils, monocyte-derived dendritic cells (DCs) and eosinophils to the
6.2. Tuberculosis Mycobacterium tuberculosis infection and TB development are related to inhalation exposure to tobacco smoke (van Zyl Smit et al., 2010) and 7
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Declaration of competing interest
household air pollution (Kolappan, 2009). Systematic reviews and meta-analyses indicate that smokers are more likely to be infected with TB and to progress to active disease (RR of ~1.5 for latent TB infection and RR of ~2.0 for TB disease) (Slama et al., 2007; Chan et al., 2014; Lin and Murray, 2007), while biomass exposure increases the risk of TB with an OR of 1.7 (95% CI 1.0–2.9) (Kolappan, 2009). ETS has been showed to dampen alveolar macrophages and neutrophils function against TB infection. Decreased Th1 number and IFN-r production, as well as enhanced Treg function, are also potential mechanisms by which smoking can facilitate TB infection (Dogar OF et al., 2015). Although PM2.5 exposure in-vitro doesn't affect M. tuberculosis phagocytosis by AM, in-vivo urban airborne particle exposure does reduce cytokines production, including IL-1β, TNF-α, from human bronchoalveolar cells and peripheral blood mononuclear cells, resulting in an alteration of M. tuberculosis defense (Torres et al., 2019).
This study is supported by NSFC 81800019, 81970020, 81770025 and program of National Innovative Research Team of High-level Local Universities in Shanghai. No conflict of interest. References Abramson, M.J., Koplin, J., Hoy, R., Dharmage, S.C., 2015. Population-wide preventive interventions for reducing the burden of chronic respiratory disease. Int. J. Tuberc. Lung Dis. 19 (9), 1007–1018. Accordini, S., Calciano, L., Johannessen, A., Portas, L., Benediktsdottir, B., Bertelsen, R.J., et al., 2018. A three-generation study on the association of tobacco smoking with asthma. Int. J. Epidemiol. 47 (4), 1106–1117. Alghamdi, M.A., Shamy, M., Redal, M.A., Khoder, M., Awad, A.H., Elserougy, S., 2014. Microorganisms associated particulate matter: a preliminary study. Sci. Total Environ. 479, 109–116. Ando, M.W.K., Seki, N., Tamakoshi, A., Suzuki, K., Ito, Y., et al., 2003. Attributable and absolute risk of lung cancer death by smoking status: findings from the Japan Collaborative Cohort study. 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7. Prevention Prohibition of smoking indoor can significantly decrease indoor PM2.5 (Semple et al., 2019). In 1998, WHO introduced the MPOWER measures to help countries to control tobacco use. The MPOWER includes (Thatcher et al., 2019) Monitor tobacco use and prevention policies (Xu et al., 2016), Protect people from tobacco smoke (Abramson et al., 2015), Offer help to quit tobacco use (Kauneliene et al., 2018), Warn about the dangers of tobacco (Muller et al., 2011), Enforce bans on tobacco advertising, promotion and sponsorship, and (Roemer et al., 2004) Raise taxes on tobacco. As of 2017, 121 countries have put at least one of WHO MPOWER measures into place at the highest level to protect people from tobacco. In the US, with the legislation of clean indoor air laws and increase of tobacco excise taxes, quitting increased, and daily smoking decreased significantly (Mojtabai et al., 2019). Moreover, tobacco control policies at national levels in Europe have been found to increase individual-level willingness to stop smoking in the home (Stevenson et al., 2017). Smoke-free homes have been recognized as an effective strategy for protecting non-smokers, especially children, against passive exposure to ETS. Supporting the establishment of smoke-free homes has been showed to be effective for the cessation of tobacco smoking.
8. Conclusion Tobacco smoking is the most important resource of indoor PM2.5. Since people spend more time indoors, indoor PM2.5 has a more critical role than outdoor PM2.5 in the development of chronic lung diseases. Epidemiology studies showed the exposure of ETS and PM2.5 were both risk factors for chronic lung diseases, especially for lung cancer, asthma and COPD. While for ILD and tuberculosis, the results were not that even. Until now, there is no epidemiology study about the PM2.5 only resourced from tobacco smoke, which should be necessary to conduct in the future. With the development of e-cigarettes and IQOS devices, more studies about the respiratory effect of these products may also need to be conducted. The mechanism of ETS and PM2.5 inducing chronic lung diseases is complicated and differs in each disease. Why do people exposed to the same risk factor develop different diseases? The crosstalk of environmental risk factors and genetic susceptibility will always be an interesting topic.
Author contributions Yingmeng Ni: Writing - original draft. Guochao Shi: Writing - original draft. Jieming Qu: Writing – review and editing 8
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